Exogenous autoinducer-2 inhibits biofilm development of Desulfovibrio sp. Huiquan2017

Exogenous autoinducer-2 inhibits biofilm development of Desulfovibrio sp. Huiquan2017
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外源自诱导剂 2 抑制脱硫弧菌属生物膜的发育。

DOI:
10.1007/s11274-021-03071-w
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发表时间:
2021-06
影响因子:
4.1
通讯作者:
Zhang Dun
Zhang Dun
中科院分区:
工程技术3区
文献类型:
--
作者:
Li Ee;Wu Jiajia;Zhang Dun

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硫酸盐还原菌(SRB)是微生物影响腐蚀的罪魁祸首,生物膜被认为在 SRB 引起的腐蚀中发挥着重要作用。然而,人们对SRB生物膜的调控知之甚少。群体感应信号分子酰基高丝氨酸内酯 (AHL) 和自诱导剂-2 (AI-2) 调节许多细菌的生物膜形成。在本研究中,一种 SRB 菌株 Desulfovibrio sp. 生产 AHL 和 AI-2。检测Huiqua2017,探讨外源AI-2对细菌生物膜形成的影响。结果发现,Desulfovibrio sp. 的无细胞上清液。 Huiquan2017 在 ΔluxS 突变菌株哈维弧菌 BB170 中诱导发光,表明该细菌产生了功能性 AI-2。在外源 AI-2 存在的情况下,Desulfovibrio sp 的生长。汇泉2017及早期生物膜形成未受影响,但后期生物膜发育受到明显抑制。生物膜变得更松、更小、更薄,并且含有更少的细菌和细胞外聚合物(EPS)。 AI-2对脱硫弧菌生物膜发育的抑制作用。 Huiquan2017主要是通过减少生物膜中EPS的量来实现的。这些发现揭示了 SRB 的生物膜调节。
Sulfate-reducing bacteria (SRB) are culprits for microbiologically influenced corrosion, and biofilms are believed to play essential roles in the corrosion induced by SRB. However, little is known about the regulation of SRB biofilms. Quorum sensing signal molecules acyl-homoserine lactones (AHLs) and autoinducer-2 (AI-2) regulate biofilm formation of many bacteria. In this study, the production of AHLs and AI-2 by one SRB strain, Desulfovibrio sp. Huiquan2017, was detected, and the effect of exogenous AI-2 on bacterial biofilm formation was discussed. It was found that the cell-free supernatants of Desulfovibrio sp. Huiquan2017 induced luminescence in a ∆luxS mutant strain Vibrio harveyi BB170, indicating the production of functional AI-2 by the bacterium. In the presence of exogenous AI-2, the growth of Desulfovibrio sp. Huiquan2017 and early biofilm formation were not affected, but the later stage of biofilm development was inhibited significantly. The biofilms became looser, smaller, and thinner, and contained less bacteria and extracellular polymeric substances (EPS). The inhibition effect of AI-2 on the biofilm development of Desulfovibrio sp. Huiquan2017 was mainly achieved through reducing the amount of EPS in biofilms. These findings shed light on the biofilm regulation of SRB.
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